Chlamydomonas, like other organisms, regulates iron assimilation very tightly through differential expression of iron assimilation components. Nevertheless, in the presence of excess iron, cells do overaccumulate iron but without an evident phenotype. As iron toxicity is attributed to reactive oxygen species, we tested the impact of photon flux density (PFD) on cells with increased iron content. We noted that growth at >500 μmol m−2 s−1 is inhibited as iron content of the medium is increased, suggesting that high light exacerbates the systems of iron toxicity and vice versa. Cells grown in high light selectively down-regulate the abundance of iron assimilation components, ferroxidase and FEA1, and storage protein ferritin1. At the RNA level, the abundance of ferroxidase (FOX1), iron reductase (FRE1), iron assimilatory protein (FEA1) and ferritin (FER1) mRNAs is also decreased. The time course of the response to high light compared to the response to Rose Bengal and H2O2 treatments suggests that both singlet oxygen and H2O2 may be implicated in the high light response. This hypothesis is supported by the recapitulation of some but not all of the high light responses in the carotenoid-deficient, high light–sensitive npq1lor1 strain. We conclude that responses to iron nutrition and PFD are connected, and the determination of an optimum for photosynthetic growth for each is dependent on the other. This work defines a fourth stage of iron nutrition in Chlamydomonas, the iron excess situation, which can be molecularly and physiologically distinguished from the iron-limited, iron-deficient and iron-replete stages, described previously.
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